ACLS -- Sign In Page Research on familial hyperhomocysteinemia first suggested that elevated circulating levels of homocysteine (Hcy) were linked to atherosclerotic vascular http://www.annclinlabsci.org/cgi/content/full/34/2/175
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Dr. Rose's Peripheral Brain--CAD RISK FACTORS hyperhomocysteinemia. Severely increased levels in homocystinuria associated with accelerated atherosclerosis; Moderately increased concentrations of http://faculty.washington.edu/momus/PB/cadriskf.htm
Extractions: CAD RISK FACTORS n.b. For purposes of guiding management of dyslipidemias, NCEP specifies a small list of risk factors as countingSee under " Dyslipidemias " for details. The NCEP recommends counting CAD risk factors among those in the "major" category below, though sedentary lifestyle and dyslipidemias in general aren't counted; HDL < 35 counts as a risk factor, though; Also, HDL > 59 counts as a "negative" risk factor, i.e. if it's there, you subtract 1 from the count of risk factors MAJOR (per JAMA 269:3015, 1993): Smoking Hypertension Dyslipidemias (high LDL, low HDL, high TC/HDL or LDL/HDL ratio) Diabetes Mellitus Unknown whether glycemic control affects risk Raises risk more for women than for men (NEJM 332:1758, 1995-rvw) Sedentary lifestyle OTHERS: High HDL (> 60mg/dl) is a "negative" risk factor per NCEP (see under " dyslipidemias ") Obesity Traditionally considered a weak but significant independent factor; may contribute secondarily through effects on glucose metabolism, BP, etc. 115,000 women enrolled in Nurses' Health study 30-55yo and free of CV disease or Ca at enrollment followed for 16y. In multivariate analysis (adjusted for age, tobacco consumption, menopausal status, use of OCP's and postmenopausal HRT, and parental h/o MI before age 60), the following results were obtained
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Blood -- Sign In Page approach to establish if hyperhomocysteinemia is a cause or simply an effect of the disease. Indeed, hyperhomocysteinemia is not a monogenic condition, http://www.bloodjournal.org/cgi/content/full/105/8/3382-a
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HONselect Pulmonary Embolism in a Patient With Pernicious Anemia and Our report highlights the thrombotic risk of hyperhomocysteinemia secondary to We believe that the hyperhomocysteinemia associated with the PA may have http://129.195.254.70/cgi-bin/HONselect?browse C18.452.648.066.480
Extractions: This Article Full Text Full Text (PDF) Submit a response ... Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed ... Cited by other online articles PubMed PubMed Citation Articles by Caldera, A. Articles by Eiger, G. Chest. American College of Chest Physicians Angel Caldera, MD Jorge Mora, MD Morris Kotler, MD and Glenn Eiger, MD From the Department of Medicine (Drs. Caldera and Mora), and the Divisions of Cardiology (Dr. Kotler) and Pulmonary and Critical Care Medicine (Dr. Eiger), Albert Einstein Medical Center, Philadelphia, PA. Correspondence to: Angel Caldera, MD, Department of Medicine, Albert Einstein Medical Center, 5401 Old York Rd, Philadelphia, PA 19141; e-mail: We report the case of a 60-year-old woman with a history of ataxia who sought evaluation after a syncopal episode. A diagnostic
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Revista De Nutrição - Translate this page The treatment of hyperhomocysteinemia consists on supplementation of the vitamins This study reviews the hyperhomocysteinemia etiology on chronic renal http://www.scielo.br/scielo.php?pid=S1415-52732005000200008&script=sci_arttext&t
Www.nlm.nih.gov/cgi/mesh/2K/MB_cgi?term=Hyperhomoc Acute methionine loadinduced hyperhomocysteinemia enhances To determine the true thrombogenicity of moderate hyperhomocysteinemia and better We conclude that moderate hyperhomocysteinemia plays a role in the http://www.nlm.nih.gov/cgi/mesh/2K/MB_cgi?term=Hyperhomocysteinemia
Entrez PubMed hyperhomocysteinemia, defined as an elevated concentration of hyperhomocysteinemia was defined as a fasting homocysteine concentration and/or an http://www.jcircadianrhythms.com/pubmed/9665374
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Methylenetetrahydrofolate Reductase (MTHFR) Thermolabile Variant hyperhomocysteinemia, C677T and A1298C Mutations; MTHFR In patients with hyperhomocysteinemia, followup testing for the MTHFR mutation might be http://www.labcorp.com/datasets/labcorp/html/chapter/mono/mg003500.htm
Extractions: Methylenetetrahydrofolate Reductase (MTHFR) Thermolabile Variant, DNA Analysis Number CPT Related Information Factor II (Prothrombin), DNA Analysis Factor V Leiden Mutation Analysis Thrombotic Risk Profile, DNA Synonyms Hyperhomocysteinemia, C677T and A1298C Mutations; MTHFR Specimen Whole blood, buccal swab (The buccal swab collection kit contains instructions for the use of a buccal swab.) Volume 7 mL whole blood (EDTA) or buccal swab kit Minimum Volume 3 mL whole blood (EDTA) or two buccal swabs Container Lavender-stopper (EDTA) or yellow-stopper (ACD) tube, LabCorp buccal swab kit Storage Instructions Maintain specimen at room temperature or refrigerate. Causes for Rejection Frozen specimen; hemolyzed; quantity not sufficient for analysis; improper container; one buccal swab Use Follow-up evaluation in individuals with hyperhomocysteinemia; evaluation of patients with venous thrombosis Limitations This assay detects only the C677T and A1298C mutations in the MTHFR gene. The diagnosis of hyperhomocysteinemia can not rely on DNA testing alone but should take into consideration clinical findings and other studies, such as serum homocysteine levels. Methodology Polymerase chain reaction (PCR) and restriction enzyme analysis Additional Information Hyperhomocysteinemia has been found in women who have experienced two or more early pregnancy losses, placental infarction and fetal growth retardation, but MTHFR mutation as a cause for early pregnancy loss is still controversial. Homozygosity for C677T has been shown to have a 2 to 3-fold increased risk for neural tube defects (NTDs) such as anencephaly and spina bifida, and compound heterozygosity for C677T and A1298C may also be a risk factor for NTDs. Dietary folic acid supplementation before the fourth week of gestation is well documented in reducing the recurrence risk for open neural tube defects by approximately 75%. It may act by normalizing homocysteine levels.
Extractions: This Article Full Text Full Text (PDF) Purchase Article ... Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager ... Request Permissions PubMed PubMed Citation Articles by Gamble, M. V Articles by Graziano, J. H American Journal of Clinical Nutrition, Vol. 81, No. 6, 1372-1377, June 2005 American Society for Clinical Nutrition Mary V Gamble Habibul Ahsan Xinhua Liu Pam Factor-Litvak Vesna Ilievski Vesna Slavkovich Faruque Parvez and Joseph H Graziano From the Departments of Environmental Health Sciences (MVG, VI, VS, FP, and JHG), Epidemiology (HA and PF-L), and Biostatistics (XL), Mailman School of Public Health, and the Department of Pharmacology, College of Physicians and Surgeons (JHG), Columbia University, New York, NY, and the New York State Psychiatric Institute, New York, NY (XL) Background: Indian Asian men residing in the United Kingdom have a higher prevalence of hyperhomocysteinemia than do their European counterparts. This has been largely attributed to dietary
Extractions: This Article Full Text Full Text (PDF) Purchase Article ... Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager ... Request Permissions PubMed PubMed Citation Articles by Amouzou, E. K American Journal of Clinical Nutrition, Vol. 79, No. 4, 619-624, April 2004 American Society for Clinical Nutrition Emile K Amouzou Charles E Adjalla Christian Villaume Ambaliou Sanni and Background: Moderate hyperhomocysteinemia is a risk for neural tube defect and neurodegenerative and vascular diseases and has nutritional, metabolic, and genetic determinants. Its prevalence in sub-Saharan Africa remains unknown. Objective: Our goal was to evaluate the prevalence of hyperhomocysteinemia and the influence of nutritional, metabolic, and genetic determinants
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Extractions: Elevations in homocyst(e)ine are typically caused either by genetic defects in the enzymes involve in homocysteine metabolism or by nutritional deficiencies in vitamin co-factors. Thus, reduction in activity of MS, MTHFR, or CbS, or decreased availability of their co-factors, vitamin B12, folic acid or vitamin B6 respectively, can cause hyperhomocyst(e)inemia. Defects of betaine homocysteine methylene transferase have not been described in literature. Homocyst(e)ine levels are higher in men than in women, both fasting and post methionine loading, and usually higher in postmenopausal rather than premenopausal women. Homocyst(e)ine also rises with age even when allowance is made for age-related increase in creatinine and decreasing vitamin levels. The rise may be related to age induced reduction in the function of MS or CbS. Other conditions that may be associated with hyperhomocyst(e)inemia are hypothyroidism, impaired kidney function, systemic lupus erythematosus and certain medications, e.g., nicotinic acid, nitrous oxide exposure, theophylline, methotrexate, and L-dopa.